Gates R J, Lazarus N R
Horm Res. 1977;8(4):189-202. doi: 10.1159/000178800.
Intraperitoneal injections of avian pancreatic polypeptide (APP) and bovine pancreatic polypeptide (BPP) are capable of returning to normal the hyperinsulinaemia, hyperglycaemia and weight gain of New Zealand obese mice. The lag glucose tolerance also becomes indistinguishable from normal. The mechanism whereby these polypeptides cause reversion is not known. Reversion can also be brought about by the intraperitoneal implantation of islets from white mice into New Zealand obese animals. The implanted islets secrete mouse pancreatic polypeptide. We conclude that the New Zealand obese syndrome arises from a genetic lack of mouse pancreatic polypeptide. We suggest that in humans a lack of pancreatic polypeptide might manifest as a syndrome analogous to that found in New Zealand obese mice.
腹腔注射禽胰多肽（APP）和牛胰多肽（BPP）能够使新西兰肥胖小鼠的高胰岛素血症、高血糖症和体重增加恢复正常。滞后的葡萄糖耐量也变得与正常无异。这些多肽导致恢复正常的机制尚不清楚。将白色小鼠的胰岛腹腔内植入新西兰肥胖动物体内也能实现恢复正常。植入的胰岛分泌小鼠胰多肽。我们得出结论，新西兰肥胖综合征是由于遗传上缺乏小鼠胰多肽所致。我们认为，在人类中，缺乏胰多肽可能表现为一种类似于在新西兰肥胖小鼠中发现的综合征。
